Finally, an additional test was added for the interaction term.
Therefore, for a Bonferroni correction on the P-values, we used P = 0.05/(2 × (4 + 4) + 1) = 0.003 as a threshold of significance. We applied the false discovery rate (FDR) to quantify uncertainty across the citation multiple hypotheses tested in the three single marker tests and the multiple sellckchem haplotype tests. The FDR q-value was therefore calculated, which denotes the expected proportion of false negatives among multiple findings. Based on the single marker and haplotype association results, the q-value Inhibitors,research,lifescience,medical for each of these nonindependent tests was calculated using the step-up procedure (Benjamini and Hochberg 1995). The q-value calculated in this way has been shown to retain desirable properties for multiple related tests in genetic association studies and can be intuitively interpreted in terms of posterior error probability. Statistical power to detect associations was estimated using the Inhibitors,research,lifescience,medical Genetic Power Calculator (http://pngu.mgh.harvard.edu/purcell/gpc/). Thus, we determined that the SZ sample (N = 79) Inhibitors,research,lifescience,medical had 41% power to detect a risk allele with 20% frequency
using an additive genotype model at alpha of 0.003. The BD sample (N = 109) had 52% power using the same criteria. The entire sample had 67% power. Results Single markers analysis Three PIK3C3 gene variants (two SNPs: rs3813065 and rs8095411 and one microsatellite, a CA-repeat) and one BDNF gene variant (rs6265) were analyzed. Single marker Inhibitors,research,lifescience,medical association analysis detected a significant difference in genotype and allelic distributions of the PIK3C3 -432C>T (rs3813065) between BD patients and controls (P = 0.025, P = 0.028, respectively) (Table 2). This difference was mainly accounted for by lower frequencies
of CT genotype and T-allele in BD than in controls. However, this association did not hold after Bonferroni correction for multiple testing. No other association was significant either for BDNF or PI3KC3 variants (Table 2). For the microsatellite variant, genotyping analysis revealed Inhibitors,research,lifescience,medical length polymorphisms in this (CA)n repeat, with n ranging from 11 to 18. The most frequent alleles were (CA)13 (56.4%), (CA)16 (18.8%), (CA)18 (14.9%), (CA)12 (3.2%), (CA)17 (3.2%), (CA)14 (2.1%), and (CA)11 (1.4%) (Information Cilengitide not displayed), but no association was significant either for BD or SZ. Table 2 Allele and genotype distribution in SZ, BD, and control subjects for three polymorphisms of BDNF and PI3KC3 genes Haplotype analysis Omnibus tests comprising the three polymorphic markers, that is microsatellite, rs3813065, and rs8095411, from the 5′ to the 3′ end of the PIK3C3 gene, showed significant differences in the overall haplotype distribution between controls and SZ (omnibus test: P = 0.030, X2 = 13.96, df = 6), controls and BP (omnibus test: P = 0.017, X2 = 17.02, df = 7), and controls and all patients (SZ + BP) (omnibus test: P = 0.016, X2 = 18.84, df = 8).
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